Chemical-induced changes in hepatic vascular innervation.

The aim of this work was to reveal the chemical-induced consequences of reversible and irreversible liver injury on the neural elements of liver vessels and to study the means of adaptation of the neuro-vascular unit to the compensatory changes during functional demands in the process from damage to regeneration. The effects of selective and non-specific hepatotoxic agents were studied in rats in acute and long-term poisoning. Acute intoxication with chemicals causing no obvious tissue destruction resulted in a decrease in the number of detectable monoaminergic nerve terminals and dense core vesicles of axons, and an increase in number of mast cells, in acute poisoning upon the effect of chemicals axondegeneration was not found. Long-term alcohol intoxication brought about hyperinnervation in the liver, decrease in blood pressure and hepatic arterial blood flow. The decrease in hepatic arterial blood flow due to noradrenaline was significantly less than in the control. During different stages of long-term carbon tetrachloride poisoning the alterations of hepatic innervation in the central and peripheral area of macroscopic liver lobe were not uniform. It is concluded that the experimentally altered environment transforms the target organ, which, in turn, can be regulated only by an adequately altered control unit. However, the functional-morphological unit operating compensatorily by means of a new innervation may respond to extraneuronal transmitters with a reaction different from that of the normal tissue.